Abstract
Pathogenic ESBL-producing E. coli lineages occur frequently worldwide, not only in a human health context but in animals and the environment, also in settings with low antimicrobial pressures. This study investigated the fitness costs of ESBL-plasmids and their influence on chromosomally encoded features associated with virulence, such as those involved in the planktonic and sessile behaviors of ST131 and ST648 E. coli. ESBL-plasmid-carrying wild-type E. coli strains, their corresponding ESBL-plasmid-“cured” variants (PCV), and complementary ESBL-carrying transformants were comparatively analyzed using growth curves, Omnilog® phenotype microarray (PM) assays, macrocolony and biofilm formation, swimming motility, and RNA sequence analysis. Growth curves and PM results pointed toward similar growth and metabolic behaviors among the strains. Phenotypic differences in some strains were detected, including enhanced curli fimbriae and/or cellulose production as well as a reduced swimming capacity of some ESBL-carrying strains, as compared to their respective PCVs. RNA sequencing mostly confirmed the phenotypic results, suggesting that the chromosomally encoded csgD pathway is a key factor involved. These results contradict the hypothesis that ESBL-plasmid-carriage leads to a fitness loss in ESBL-carrying strains. Instead, the results indicate an influence of some ESBL-plasmids on chromosomally encoded features associated with virulence in some E. coli strains. In conclusion, apart from antibiotic resistance selective advantages, ESBL-plasmid-carriage may also lead to enhanced virulence or adaption to specific habitats in some strains of pandemic ESBL-producing E. coli lineages.
Highlights
The global emergence of antimicrobial resistance, including extended-spectrum beta-lactamases (ESBL), is driven by plasmids encoding for these factors, but is crucially influenced by pandemic bacterial clonal lineages (Naseer and Sundsfjord, 2011)
To assess the possibility of interactions between ESBL-plasmids and chromosomal content, we conducted a study using an unconventional approach by constructing plasmid-“cured” variants (PCV) of ESBL-plasmid-carrying WT strains of ST131 and ST648
In Phenotype Microarray (PM) assays, which are a consolidation of regular LB growth curve tests (Supplementary Table S2), significant differences were detected in select wells
Summary
The global emergence of antimicrobial resistance, including extended-spectrum beta-lactamases (ESBL), is driven by plasmids encoding for these factors, but is crucially influenced by pandemic bacterial clonal lineages (Naseer and Sundsfjord, 2011). Besides ST131, several STs, including ST648, ST617, ST167, ST410, ST224, and ST117, appear to be associated with ESBLproduction, which demonstrates that ESBL-producing isolates are not distributed over all phylogenetic backgrounds (Ewers et al, 2012). This is expected in cases of solely plasmiddriven spread (Ewers et al, 2012). Prior studies suggest trade-offs between antibiotic-resistance and fitness in such strains (Dasilva and Bailey, 1986; Lenski, 1997; Andersson and Hughes, 2010) This does not necessarily apply to ST131 and ST648. These include fertility and virulence factors, genes for plasmid maintenance including toxin-antitoxin systems, resistances against heavy metals (Seiler and Berendonk, 2012; Schaufler et al, 2013), and putative protein-coding genes (Smet et al, 2010b)
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